DACT1 overexpression inhibits proliferation, enhances apoptosis, and increases daunorubicin chemosensitivity in KG-1α cells
DACT1 has been shown to participate in the development of many types of tumors; however, its role and precise molecular mechanisms in leukemia are unclear. In this study, we investigated the effect of DACT1 on KG-1α leukemia cells to further understand the mechanisms of DACT1-mediated tumor suppress...
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| Format: | Article |
| Language: | English |
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SAGE Publishing
2017-09-01
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| Series: | Tumor Biology |
| Online Access: | https://doi.org/10.1177/1010428317711089 |
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| _version_ | 1849417316596449280 |
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| author | Ke Zhu Benchun Jiang Ying Yang Rong Hu Zhuogang Liu |
| author_facet | Ke Zhu Benchun Jiang Ying Yang Rong Hu Zhuogang Liu |
| author_sort | Ke Zhu |
| collection | DOAJ |
| description | DACT1 has been shown to participate in the development of many types of tumors; however, its role and precise molecular mechanisms in leukemia are unclear. In this study, we investigated the effect of DACT1 on KG-1α leukemia cells to further understand the mechanisms of DACT1-mediated tumor suppression. We transfected a DACT1 expression plasmid to upregulate DACT1 in KG-1α cells and analyzed the resulting phenotypic changes. The results demonstrated that DACT1 overexpression inhibited KG-1α proliferation, increased apoptosis, and arrested cells in the G0/G1 phase. Mechanistically, DACT1 overexpression inhibited Wnt/β-catenin signaling by reducing nuclear β-catenin levels in KG-1α cells. Furthermore, the viability of KG-1α cells transfected with DACT1 was significantly reduced when treated with daunorubicin. We also found that DACT1 reduced P-glycoprotein expression in KG-1α cells. These findings revealed an inhibitory role for DACT1 in leukemogenesis and provided evidence that DACT1 is an attractive target for the development of novel anti-leukemia therapies. |
| format | Article |
| id | doaj-art-1090042a722f4974a2fca9f4e548491f |
| institution | Kabale University |
| issn | 1423-0380 |
| language | English |
| publishDate | 2017-09-01 |
| publisher | SAGE Publishing |
| record_format | Article |
| series | Tumor Biology |
| spelling | doaj-art-1090042a722f4974a2fca9f4e548491f2025-08-20T03:32:54ZengSAGE PublishingTumor Biology1423-03802017-09-013910.1177/1010428317711089DACT1 overexpression inhibits proliferation, enhances apoptosis, and increases daunorubicin chemosensitivity in KG-1α cellsKe Zhu0Benchun Jiang1Ying Yang2Rong Hu3Zhuogang Liu4Department of Hematology, Shengjing Hospital of China Medical University, Shenyang, ChinaDepartment of General Surgery, Shengjing Hospital of China Medical University, Shenyang, ChinaDepartment of Hematology, Shengjing Hospital of China Medical University, Shenyang, ChinaDepartment of Hematology, Shengjing Hospital of China Medical University, Shenyang, ChinaDepartment of Hematology, Shengjing Hospital of China Medical University, Shenyang, ChinaDACT1 has been shown to participate in the development of many types of tumors; however, its role and precise molecular mechanisms in leukemia are unclear. In this study, we investigated the effect of DACT1 on KG-1α leukemia cells to further understand the mechanisms of DACT1-mediated tumor suppression. We transfected a DACT1 expression plasmid to upregulate DACT1 in KG-1α cells and analyzed the resulting phenotypic changes. The results demonstrated that DACT1 overexpression inhibited KG-1α proliferation, increased apoptosis, and arrested cells in the G0/G1 phase. Mechanistically, DACT1 overexpression inhibited Wnt/β-catenin signaling by reducing nuclear β-catenin levels in KG-1α cells. Furthermore, the viability of KG-1α cells transfected with DACT1 was significantly reduced when treated with daunorubicin. We also found that DACT1 reduced P-glycoprotein expression in KG-1α cells. These findings revealed an inhibitory role for DACT1 in leukemogenesis and provided evidence that DACT1 is an attractive target for the development of novel anti-leukemia therapies.https://doi.org/10.1177/1010428317711089 |
| spellingShingle | Ke Zhu Benchun Jiang Ying Yang Rong Hu Zhuogang Liu DACT1 overexpression inhibits proliferation, enhances apoptosis, and increases daunorubicin chemosensitivity in KG-1α cells Tumor Biology |
| title | DACT1 overexpression inhibits proliferation, enhances apoptosis, and increases daunorubicin chemosensitivity in KG-1α cells |
| title_full | DACT1 overexpression inhibits proliferation, enhances apoptosis, and increases daunorubicin chemosensitivity in KG-1α cells |
| title_fullStr | DACT1 overexpression inhibits proliferation, enhances apoptosis, and increases daunorubicin chemosensitivity in KG-1α cells |
| title_full_unstemmed | DACT1 overexpression inhibits proliferation, enhances apoptosis, and increases daunorubicin chemosensitivity in KG-1α cells |
| title_short | DACT1 overexpression inhibits proliferation, enhances apoptosis, and increases daunorubicin chemosensitivity in KG-1α cells |
| title_sort | dact1 overexpression inhibits proliferation enhances apoptosis and increases daunorubicin chemosensitivity in kg 1α cells |
| url | https://doi.org/10.1177/1010428317711089 |
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